The plasma level and biomarker value of neutrophil gelatinase-associated lipocalin in critically ill patients with acute kidney injury are not affected by continuous venovenous hemofiltration and anticoagulation applied

Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury (AKI), and levels reflect severity of disease in critically ill patients. However, continuous venovenous hemofiltration (CVVH) may affect plasma levels by clearance or release of NGAL by activated neutrophils in...

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Published in:Critical care (London, England) England), 2014-04, Vol.18 (2), p.R78-R78
Main Authors: Schilder, Louise, Nurmohamed, S Azam, ter Wee, Pieter M, Paauw, Nanne J, Girbes, Armand R J, Beishuizen, Albertus, Beelen, Robert H J, Groeneveld, A B Johan
Format: Article
Language:English
Subjects:
Acute Kidney Injury - blood
Acute Kidney Injury - mortality
Acute Kidney Injury - therapy
Acute-Phase Proteins
Adult
Aged
Aged, 80 and over
Anticoagulants - therapeutic use
Biomarkers - blood
Critical Illness - therapy
Female
Hemofiltration - methods
Humans
Lipocalin-2
Lipocalins - blood
Male
Middle Aged
Prospective Studies
Proto-Oncogene Proteins - blood
Survival Rate - trends
Treatment Outcome
Young Adult
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Summary:Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury (AKI), and levels reflect severity of disease in critically ill patients. However, continuous venovenous hemofiltration (CVVH) may affect plasma levels by clearance or release of NGAL by activated neutrophils in the filter, dependent on the anticoagulation regimen applied. We therefore studied handling of NGAL by CVVH in patients with AKI. Immediately before initiation of CVVH, prefilter blood was drawn. After 10, 60, 180, and 720 minutes of CVVH, samples were collected from pre- and postfilter (in- and outlet) blood and ultrafiltrate. CVVH with the following anticoagulation regimens was studied: no anticoagulation in case of a high bleeding tendency (n = 13), unfractionated heparin (n = 8), or trisodium citrate (n = 21). NGAL levels were determined with enzyme-linked immunosorbent assay (ELISA). Concentrations of NGAL at inlet and outlet were similar, and concentrations did not change over time in any of the anticoagulation groups; thus no net removal or production of NGAL occurred. Concentrations of NGAL at inlet correlated with disease severity at initiation of CVVH and at the end of a CVVH run. Concentrations of NGAL in the ultrafiltrate were lower with citrate-based CVVH (P = 0.03) and decreased over time, irrespective of anticoagulation administered (P 
ISSN:1364-8535
1466-609X
DOI:10.1186/cc13838